Redox imbalance in infertility and assisted reproduction: biomarkers, mechanisms, multi-omics integration, and personalised therapeutic strategies
Abstract
Redox biology occupies a central but paradoxical role in human reproduction. Reactive oxygen species (ROS) are indispensable mediators of sperm capacitation, oocyte activation, embryo development, and trophoblast invasion, yet excessive ROS generation causes oxidative stress that damages gametes, impairs preimplantation development, and compromises implantation. Conversely, reductive stress, an emerging but still underappreciated state in which antioxidant defences exceed physiological need, may suppress the low-level ROS signalling required for normal reproductive function. Despite decades of mechanistic research, clinical translation has been limited by the absence of standardised redox phenotyping and by the widespread use of empirical antioxidant supplementation, the benefits of which remain unproven in adequately powered randomised controlled trials. This review synthesises current evidence on the dual-pole redox continuum in infertility and assisted reproductive technology, with emphasis on the mechanistic pathways through which oxidative and reductive stress affect male reproductive function, ovarian and oocyte competence, endometrial receptivity, and preimplantation embryo development. It also critically examines the clinical failure of non-stratified antioxidant trials and evaluates the diagnostic potential of redox biomarkers and multi-omics approaches, including oxidation-reduction potential measurement, metabolomics, transcriptomics, and proteomics, for…
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